EFFECT OF HYDROXYL RADICAL SCAVENGING ON ENDOTOXIN-INDUCED LUNG INJURY

  • 1 January 1985
    • journal article
    • research article
    • Vol. 97  (3) , 300-307
Abstract
The release of oxygen radicals, in particular the hydroxyl radical, from sequestered neutrophils produces acute lung injury after a number of insults. The purpose was to determine whether hydroxyl radical, OH., is responsible for the lung injury from endotoxin characterized by pulmonary leukostasis, increased thromboxane (Tx) production leading to pulmonary hypertension and hypoxia and increased protein permeability. This hypothesis was tested by infusion of a selective OH. scavenger, dimethyl thiourea (0.75 g/kg), into unanesthetized sheep before endotoxin and comparison of the response to that seen with endotoxin alone. Pulmonary vascular integrity was measured by the use of lung lymph flow, QL and lymph protein transport. TxA2 was measured as TxB2 and prostacyclin as 6-keto-PG[prostaglandin]F1.alpha.. No difference was found in the degree of leukopenia and hypoxia after endotoxin or the levels of TxB2, 6-keto-PGF1.alpha. and pulmonary hypertension with dimethyl thiourea, compared with endotoxin alone. The permeability injury was also identical, with a 2- to 3-fold increase in protein-rich lymph seen in both groups. It appears that OH. does not play a major causative role in either phase of endotoxin lung injury.